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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Sodium depletion which occurred in cattle following exteriorization of a parotid duct produced depression of both plasma and salivary sodium, acidosis, elevated plasma aldosterone and renin activity. Increased sodium appetite, characteristic of sodium depletion, was assessed by operant behaviour where scoring of panel pressing for NaHCO(3) rewards showed change in sodium appetite.2. Sodium-depleted calves readily drank the calculated ionic deficit as a hypertonic solution (4 l.) in a few minutes, or as an isotonic solution (16 l.) usually within 30 min.3. When the ionic deficit was restored by either i.v. infusion or drinking, sodium appetite was reduced significantly. The suppression of sodium appetite was more rapid when the depleted ions were replaced by drinking (30 min) than by i.v. infusion (2 hr) but in both circumstances the effect was short lived since sodium appetite redeveloped within 3 hr.4. The rapid return of sodium appetite following restoration of the ionic deficit occurred even when the plasma sodium level was normal. Other biochemical changes resulting from sodium depletion, such as acidosis and reduced salivary sodium, could not be correlated with variation in sodium appetite.5. Rapid infusion of Ringer saline (4 l.) did not inhibit the sodium appetite, which suggests that neither vascular volume changes per se nor vascular baroreceptors control sodium appetite in sodium-deficient calves.Plasma aldosterone fell rapidly following infusion of the hypertonic solution but only slightly with the isotonic infusion. The change in plasma hormone level was not related to changes in sodium appetite.6. Drinking the hypertonic solution produced a marked reduction in panel pressing for NaHCO(3) with a rapid rise in plasma sodium. Consumption of the larger volume of isotonic solution also inhibited sodium intake but plasma sodium remained low. A secondary increase in plasma renin activity (p.r.a.) occurred following ingestion of the hypertonic solution, but both p.r.a. and aldosterone fell to normal levels over the next 6 hr when the cattle again showed marked sodium appetite. It is possible that these effects may be due to ion and fluid movement between gut and extracellular fluid and reflect osmolality changes or tissue dehydration.7. It is concluded that the sodium appetite of sodium deficient cattle is only temporarily alleviated by restoration of the depleted ionic loss, and that the behavioural response to seek sodium rewards is independent of plasma sodium, p.r.a., aldosterone and volume changes in the gut and vascular system.8. Recent reports suggest that sodium appetite may be controlled by receptors in the hypothalamus or by angiotensin II in the brain. In cattle the capacious gut may also be involved, since sodium appetite is inhibited more rapidly when the depleted ions are taken orally than by i.v. infusion.
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PMID:The effect on salt appetite and the renin-aldosterone system on replacing the depleted ions to sodium-deficient cattle. 702 8

The effect of acute administration of captopril, an angiotensin converting enzyme inhibitor, on vascular responses of rings of rat aortic smooth muscle was tested in vitro. Dose-response curves for various vasoactive agents were obtained before and after exposure to captopril (2 x 10(-4) M) for 30 minutes. In the presence of captopril, contractile responses to angiotensin I (5 x 10(-10) to 5 x 10(-8) M) were attenuated significantly, probably as a result of decreased local conversion of angiotensin I to angiotensin II. Contractile responses to angiotensin II (10(-11) to 5 x 10(-9) M) were not affected by captopril. All responses to norepinephrine (10(-9) to 10(-4) M) and phenylephrine (10(-8) to 10(-4) M) were attenuated significantly from control in the presence of captopril. In the presence of the alpha-adrenergic antagonist, phentolamine, captopril did not affect either the contractile responses to KCl (30 to 100 mM) or the isoproterenol-induced (10(-8) to 10(-5) M) relaxation of KCl-depolarized tissue. These results suggest that captopril decreased vascular responsiveness to alpha-adrenergic agonists but not to beta-adrenergic agonists. Low concentrations of bradykinin (10(-10) to 10(-8) M) induced contraction in KCl-depolarized tissue while higher concentrations (10(-7) and 10(-6) M) induced relaxation. In the presence of captopril, relaxation occurred at all concentrations of bradykinin (10(-10) to 10(-6) M), probably as a result of decreased degradation of the bradykinin. These data suggest depression of alpha-adrenergic responsiveness in vascular smooth muscle as another potential antihypertensive action of captopril.
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PMID:Effect of in vitro administration of captopril on vascular reactivity of rat aorta. 703 33

1. Potassium was infused intravenously in an incremental fashion and the plasma aldosterone response were measured in conscious beagle dogs at five different intakes of dietary sodium. 2. Potassium/aldosterone dose-response curves were constructed for each dietary sodium regimen. 3. The rate of increase of plasma potassium during graded potassium infusion became progressively greater with increasing sodium depletion. 4. Regression lines of plasma aldosterone on plasma potassium were progressively elevated and steepened with increasing sodium depletion. 5. The alteration of these dose-response curves could in part have been the result of chronic elevation of plasma potassium and angiotensin II, and depression of plasma sodium, with sodium deprivation. 6. By contrast, acute changes in plasma angiotensin II or sodium concentrations across incremental infusions of potassium did not explain the progressive changes in the potassium/aldosterone dose-response curves. 7. The steepest part of the plasma aldosterone response curve was in the plasma potassium range 4-6 mmol/1. 8. Maximum achieved aldosterone levels were similar to or greater than those attained during angiotensin II infusion in previous studies in beagle dogs. 9. Potassium, like angiotensin II and adrenocorticotropic hormone, becomes a more effective stimulus to aldosterone with sodium depletion, thereby facilitating the preservation of sodium homoeostasis.
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PMID:Effect of changes in sodium balance on potassium/aldosterone dose-response curves in the dog. 706 59

During the rat oestrous cycle, cholinergic-stimulated water intake is constant across days; while both daily ad lib and angiotensin II-stimulated water intakes are least on the day of oestrus. If permitted to self select, however, rats will elect to drink sodium chloride solutions as well as water under ad lib or angiotensin-stimulated conditions. Therefore, adult female rats with continuous access to both water and 1.8% NaCl were studied to determine if saline intake also varied with the oestrous cycle. Ad lib drinking and drinking stimulated by intracerebroventricular injections of angiotensin II or carbachol were monitored daily for the duration of an entire oestrous cycle. Both ad lib and angiotensin-induced sodium intakes were depressed at oestrus, while the minimal sodium intake seen after carbachol was not changed. The depression in sodium intake so mirrored that observed for water intake that the ratio of saline to water intake did not vary over the oestrous cycle.
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PMID:Depression of ad lib and angiotensin-induced sodium intake at oestrus. 719 63

When isolated blood-perfused pig lungs are exposed to inspired O2 tensions (PIO2) below 30 Torr, hypoxic pulmonary vasoconstriction is transient. To determine whether this transience is caused by a decrease in the amount of ATP available for maintenance of smooth muscle contraction, we compared normoxic (PIO2 = 100 Torr) and hypoxic (PIO2 = 10 Torr) dose-response curves to infusions of prostaglandin F2 alpha (PGF2 alpha), angiotensin II (AII), and potassium chloride (KCl). Hypoxia caused reversible depression of the responses to PGF2 alpha and AII but had no effect on the response to KCl. Because during hypoxia the lung was capable of an undiminished vasoconstrictor response to at least one agent, it seems unlikely that the supply of ATP available for contraction was limiting. The mechanism for the transience of the vasoconstrictor response to low PO2 values and the depression of the response to AII and PGF2 alpha remains unknown, but could involve depression of ATP production sufficient to limit some energy-requiring process other than contraction or release of a vasodilator.
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PMID:Effect of severe hypoxia on the pulmonary vascular response to vasoconstrictor agents. 725 46

The response of heart function to angiotensin II (AT II) was studied in 18 patients on regular hemodialysis. The mean age was 33 years and they had been dialyzed for 55 months in the average. AT II was infused from a large vein and systolic blood pressure was raised by 40 mmHg. Before and after the change in blood pressure, M-mode echocardiogram of left ventricle was recorded. Left ventricular enddiastolic dimension, stroke index and cardiac index were found to be normal except for 9 patients who showed cardiac index above 4.0L/min/m2. No significant change was found in these parameters after the rise of blood pressure by AT II. Control ejection fraction (EF) was slightly but nonsignificantly lower in the patients than the healthy subjects; 0.73 +/- 0.13 vs. 0.80 +/- 0.05. Though significant falls in EF were found in the patient and in the healthy group, the former showed a profound depression of EF to 0.64 +/- 0.10. This value was significantly lower than the value of the latter group; 0.76 +/- 0.04 (p less than 0.01). Since none had overt heart failure, a depression of EF after AT II can be regarded as subclinical abnormality of heart function. AT II will be useful to detect this limited reserve of heart function in patients on regular hemodialysis who may show normal function at rest.
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PMID:Depression of heart function after angiotensin II infusion in patients on chronic hemodialysis. 734 Oct 21

Cods were equipped with cannulae for drainage of the stomach and for the separate perfusion of the stomach (pure seawater containing phenol red as a volume marker) and intestine (diluted seawater). Acidity of the gastric effluence was titrated, its volume calculated from the phenol red concentration. Gastric mucosal plasma flow (MPF) was estimated by gastric 14C-aniline clearance. I.m. injection of angiotensin II (AII) depressed basal acid secretion in a dose-dependent fashion. Also the MPF was reduced, but relatively less than the secretory depression. Therefore, the AII-induced secretory inhibition could not be explained by restrained mucosal blood flow. Perfusion of the intestine with diluted seawater, or a continuous i.m. infusion of 0.6% NaCl both rendered the fishes non-drinking. A high dose of AII (150 micrograms/kg . h) induced drinking in intestinally perfused cod while lower doses (15, 50 micrograms/kg . h) did not. In i.m. saline-injected cod, all three doses were dipsogenic. The results suggest that 0.6% saline infusion induces a permanent satiety and that intestinal perfusion in addition induces a preabsorptive satiety. The preabsorptive satiety appears more resistant to the dipsogenic action of AII than the permanent one.
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PMID:Effects of exogenous angiotensin II in the Atlantic cod, Gadus morhua. Observations on gastric acid secretion, gastric sham drinking and gastric mucosal plasma flow (14C-aniline clearance). 734 2

We wondered if depression of oxidative adenosine triphosphate (ATP) production caused pulmonary vasoconstriction. If so, then several chemically different inhibitors of oxidative ATP production all should cause pulmonary pressor responses. The vascular reactivity of isolated, blood-perfused rat lungs was established by eliciting pressor responses to airway hypoxia and to intraarterial angiotensin II. Then, during normoxia, we added to perfusate one of five chemical inhibitors of oxidative ATP production: 10 mM azide, 1 mM cyanide, 1 mM dinitrophenol, 5 or 10 microM antimycin A, or 0.5 microM rotenone. Each of the five chemical inhibitors, but not their solvents, caused a transient pressor response, followed by loss of vascular reactivity to hypoxia, angiotensin II, and chemical inhibitors. The inhibitor pressor responses were not due to an effect on blood cells, since they also were seen in lungs perfused with plasma. The magnitudes of pressor responses to all metabolic inhibitors except azide correlated with the magnitudes of preceding pressor responses to hypoxia, but not to the preceding angiotensin II responses. When verapamil or calcium chloride was added to perfusate, the hypoxic and inhibitor pressor responses were blunted more than was the angiotensin II response. Thus, five chemically different substances, inhibiting different steps of oxidative ATP production, all caused pressor responses that were blocked readily by verapamil and by increased perfusate calcium chloride. These results support the possibility that depression of oxidative ATP production elicits pulmonary vasoconstriction that is dependent on influx of extracellular calcium. Hypoxia might also be sensed in the pulmonary circulation by decreased oxidative ATP production in some as yet unidentified lung cell.
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PMID:Inhibitors of oxidative ATP production cause transient vasoconstriction and block subsequent pressor responses in rat lungs. 746 Feb 12

This study was designed to evaluate the functional significance of angiotensin II (Ang II) receptors identified by previous receptor autoradiography studies to be located presynaptically on terminals of dopaminergic neurones projecting to the striatum. Microdialysis was performed in the striatum of conscious freely moving rats and dopamine and serotonin metabolites measured by HPLC with electrochemical detection. During perfusion with artificial CSF, the major extracellular dopamine metabolite identified was DOPAC with smaller concentrations of HVA. When Ang II (1 microM) was introduced into the dialysis perfusion medium, DOPAC output increased markedly, peaking at 219%, and returned to control with vehicle perfusion during the recovery period. This increase in DOPAC output with Ang II was completely blocked by co-administration of the AT1 selective antagonist, Losartan (1 microM). Administration of Losartan alone led to a significant (16%) depression of DOPAC output relative to vehicle, suggesting that dopamine release is under a tonic facilitatory influence of Ang II via the AT1 receptor subtype. Parallel, but smaller changes were seen with HVA outputs. During Ang II perfusion the output of HVA was elevated 34-79% of that in vehicle-treated rats and this effect was completely abolished by concomitant administration of Losartan. As was observed with DOPAC output, administration of Losartan alone led to a 13-24% depression of HVA output compared to vehicle perfusion. When nomifensine (10 microM) was included in the infusion fluid, dopamine was clearly measurable. Ang II perfusion increased the levels of dopamine to 225%. Values returned towards baseline during the recovery period. Ang II administration also increased (by 15% and 55%) the levels of the major serotonin metabolite, 5HIAA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of angiotensin II on dopamine and serotonin turnover in the striatum of conscious rats. 751 80

Both endothelin-1 protein and endothelin-1 specific binding sites have been identified in areas of the medulla oblongata involved in respiratory control. We examined whether endothelin acting centrally affects respiratory output during early postnatal life. We initially examined the effect of intracisternally administrated endothelin on respiratory output in 10 2- to 18-day-old piglets. Endothelin-1 administration at 50 nmol to 1 mumol caused respiratory inhibition. We subsequently examined whether this response is mediated through chemosensitive areas of the ventral medulla. Endothelin-1 was microinjected into specific ventral or dorsal medullary regions in 31 14- to 22-day-old piglets. Microinjection of endothelin-1 (10 fmol to 0.1 pmol) just above the hypoglossal roots, lateral to the pyramids, and within 1 mm from the surface (n = 24) attenuated respiratory output, and complete apnea occurred with 1 pmol in all animals. However, microinjection of endothelin-1 3 mm below the ventral surface (n = 5) and into the dorsal medulla (n = 3) had no inhibitory effect. Comparable doses of angiotensin II (n = 5) and norepinephrine (n = 5) microinjected into the endothelin-1 sensitive area also did not influence respiratory output. These effects of endothelin-1 were not altered by prior endothelin-B receptor blockade (IRL-1038) but could be reversed by endothelin-A receptor blockade (BQ-610). These results suggest that endothelin-1 release may cause ventilatory depression mediated through endothelin-A receptors located in the chemosensitive areas of the ventrolateral medulla.
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PMID:Central effects of endothelin on respiratory output during development. 759 97


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